Changes in respiratory activity induced by mastication in humans

1992 ◽  
Vol 72 (2) ◽  
pp. 779-786 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
L. Viroli ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Respiratory Activity ◽  
Minute Ventilation ◽  
Respiratory Rhythm ◽  
Upper Airway ◽  
Muscular Activity ◽  
Electromyographic Activity ◽  
Complex Interactions ◽  
Inspiratory Muscles ◽  
Response To Exercise

We studied the influence of mastication on respiratory activity in nine healthy volunteers who were requested to masticate a 5-g chewing gum bolus at a spontaneous rate (SR) for 5 min and “at the maximum possible rate” (MPR) for 1 min. Significant increases in respiratory frequency were induced by SR mastication due to a decrease in both the inspiratory and expiratory time. Tidal volume displayed slight nonsignificant decreases, but minute ventilation and mean inspiratory flow significantly increased. The duty cycle (TI/TT) did not change significantly. Total airway resistance significantly increased. Both peak and rate of rise of the integrated electromyographic activity of inspiratory muscles presented marked increases, accompanied by the appearance of a low level of tonic muscular activity. Similar but more intense effects on respiratory activity were induced by MPR mastication; in addition, a significant decrease in tidal volume and a significant increase in TI/TT were observed. Rhythmic handgrip exercise performed at metabolic rates comparable to those attained during SR or MPR mastication induced similar changes in the drive and time components of the breathing pattern, although accompanied respectively by nonsignificant or significant increases in tidal volume. Furthermore, the frequency of SR mastication significantly entrained the respiratory rhythm. The results suggest that mastication-induced hyperpnea does not merely represent a ventilatory response to exercise but also reflects complex interactions between respiratory and nonrespiratory functions of the upper airway and chest wall muscles.

Effect of intestinal afferent stimulation on pattern of respiratory muscle activation

1989 ◽  
Vol 66 (3) ◽  
pp. 1455-1461 ◽  
Author(s):  
S. B. Gottfried ◽  
A. F. DiMarco
Keyword(s):  
Tidal Volume ◽  
Mechanical Stimulation ◽  
Respiratory Muscle ◽  
Muscle Activation ◽  
Upper Airway ◽  
Visceral Afferents ◽  
Electromyographic Activity ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Stimulation Of

The purpose of the present study was to examine the reflex effects of mechanical stimulation of intestinal visceral afferents on the pattern of respiratory muscle activation. In 14 dogs anesthetized with pentobarbital sodium, electromyographic activity of the costal and crural diaphragm, parasternal intercostal, and upper airway respiratory muscles was measured during distension of the small intestine. Rib cage and abdominal motion and tidal volume were also recorded. Distension produced an immediate apnea (11.16 +/- 0.80 s). During the first postapneic breath, costal (43 +/- 7% control) and crural (64 +/- 6% control) activity were reduced (P less than 0.001). In contrast, intercostal (137 +/- 11%) and upper airway muscle activity, including alae nasi (157 +/- 16%), genioglossus (170 +/- 15%), and posterior cricoarytenoid muscles (142 +/- 7%) all increased (P less than 0.005). There was greater outward rib cage motion although the abdomen moved paradoxically inward during inspiration, resulting in a reduction in tidal volume (82 +/- 6% control) (P less than 0.005). Postvagotomy distension produced a similar apnea and subsequent reduction in costal and crural activity. However, enhancement of intercostal and upper airway muscle activation was abolished and there was a greater fall in tidal volume (65 +/- 14%). In conclusion, mechanical stimulation of intestinal afferents affects the various inspiratory muscles differently; nonvagal afferents produce an initial apnea and subsequent depression of diaphragm activity whereas vagal pathways mediate selective enhancement of intercostal and upper airway muscle activation.

Ventilatory compensation for changes in functional residual capacity during sleep

1987 ◽  
Vol 62 (3) ◽  
pp. 1299-1306 ◽  
Author(s):  
R. L. Begle ◽  
J. B. Skatrud ◽  
J. A. Dempsey
Keyword(s):  
Tidal Volume ◽  
Functional Residual Capacity ◽  
Minute Ventilation ◽  
Muscle Length ◽  
Normal Subjects ◽  
Conscious State ◽  
Inspiratory Muscle ◽  
Compensatory Response ◽  
Inspiratory Muscles ◽  
Residual Capacity

The role of conscious factors in the ventilatory compensation for shortened inspiratory muscle length and the potency of this compensatory response were studied in five normal subjects during non-rapid-eye-movement sleep. To shorten inspiratory muscles, functional residual capacity (FRC) was increased and maintained for 2–3 min at a constant level (range of increase 160–1,880 ml) by creating negative pressure within a tank respirator in which the subjects slept. Minute ventilation was maintained in all subjects over the entire range of increased FRC (mean change +/- SE = -3 +/- 1%) through preservation of tidal volume (-2 +/- 2%) despite slightly decreased breathing frequency (-6 +/- 2%). The decrease in frequency (-13 +/- 2%) was due to a prolongation in expiratory time. Inspiratory time shortened (-10 +/- 1%). Mean inspiratory flow increased 15 +/- 3% coincident with an increase in the slope of the moving time average of the integrated surface diaphragmatic electromyogram (67 +/- 21%). End-tidal CO2 did not rise. In two subjects, control tidal volume was increased 35–50% with CO2 breathing. This augmented tidal volume was still preserved when FRC was increased. We concluded that the compensatory response to inspiratory muscle shortening did not require factors associated with the conscious state. In addition, the potency of this response was demonstrated by preservation of tidal volume despite extreme shortening of the inspiratory muscles and increase in control tidal volumes caused by CO2 breathing. Finally, the timing changes we observed may be due to reflexes following shortening of inspiratory muscle length, increase in abdominal muscle length, or cardiovascular changes.

Influence of global inspiratory muscle fatigue on breathing during exercise

1996 ◽  
Vol 80 (4) ◽  
pp. 1270-1278 ◽  
Author(s):  
P. Sliwinski ◽  
S. Yan ◽  
A. P. Gauthier ◽  
P. T. Macklem
Keyword(s):  
Tidal Volume ◽  
Muscle Fatigue ◽  
Minute Ventilation ◽  
Inspiratory Muscle ◽  
Abdominal Muscles ◽  
Maximal Power Output ◽  
Lung Inflation ◽  
Rib Cage ◽  
Inspiratory Muscles ◽  
Inspiratory Muscle Fatigue

We evaluated the effect of global inspiratory muscle fatigue (GF) on respiratory muscle control during exercise at 30, 60, and 90% of maximal power output in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. Esophageal and gastric pressures, anteroposterior displacement of the rib cage and abdomen, breathing pattern, and perceived breathlessness were measured. Induction of GF had no effect on the ventilatory parameters during mild and moderate exercise. It altered, however, ventilatory response to heavy exercise by increasing breathing frequency and minute ventilation, with minor changes in tidal volume. This was accompanied by an increase in perceived breathlessness. GF significantly increased both the tonic and phasic activities of abdominal muscles that allowed 1) the diaphragm to maintain its function while developing less pressure, 2) the same tidal volume with lesser shortening of the rib cage inspiratory muscles, and 3) relaxation of the abdominal muscles to contribute to lung inflation. The increased work performed by the abdominal muscles may, however, lead to a reduction in their strength. GF may impair exercise performance in some healthy subjects that is probably not related to excessive breathlessness or other ventilatory factors. We conclude that the respiratory system is remarkably adaptable in maintaining ventilation during exercise even with impaired inspiratory muscle contractility.

Influence of CO2 on upper airway muscles and chest wall/diaphragm corticomotor responses assessed by transcranial magnetic stimulation in awake healthy subjects

2012 ◽  
Vol 112 (5) ◽  
pp. 798-805 ◽  
Author(s):  
Jean-Christian Borel ◽  
Cesar Augusto Melo-Silva ◽  
Simon Gakwaya ◽  
Frédéric Sériès
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Tidal Volume ◽  
Chest Wall ◽  
Healthy Subjects ◽  
Magnetic Stimulation ◽  
Minute Ventilation ◽  
Motor Evoked Potential ◽  
Upper Airway ◽  
Random Order ◽  
Respiratory Drive

Rationale: functional interaction between upper airway (UA) dilator muscles and the diaphragm is crucial in the maintenance of UA patency. This interaction could be altered by increasing respiratory drive. The aim of our study was to compare the effects of hypercapnic stimulation on diaphragm and genioglossus corticomotor responses to transcranial magnetic stimulation (TMS). Methods: 10 self-reported healthy men (32 ± 9 yr; body mass index = 24 ± 3 kg/m−2) breathed, in random order, room air or 5% and then 7% FiCO2, both balanced with pure O2. Assessments included ventilatory variables, isoflow UA resistance (at 300 ml/s), measurement of lower chest wall/diaphragm (LCW/diaphragm), and genioglossus motor threshold (MT) and motor-evoked potential (MEP) characteristics. TMS twitches were applied during early inspiration and end expiration at stimulation intensity 30% above LCW/diaphragm and genioglossus MT. Results: compared with room air, CO2 inhalation significantly augmented minute ventilation, maximal inspiratory flow, tidal volume, and tidal volume/respiratory time ratio. UA resistance was unchanged with CO2 inhalation. During 7% CO2 breathing, LCW/diaphragm MT decreased by 9.6 ± 10.1% whereas genioglossus MT increased by 7.2 ± 9%. CO2-induced ventilatory stimulation led to elevation of LCW/diaphragm MEP amplitudes during inspiration but not during expiration. LCW/diaphragm MEP latencies remained unaltered both during inspiration and expiration. Genioglossus MEP latencies and amplitudes were unchanged with CO2. Conclusion: in awake, healthy subjects, CO2-induced hyperventilation is associated with heightened LCW/diaphragm corticomotor activation without modulating genioglossus MEP responses. This imbalance may promote UA instability during increased respiratory drive.

Breathing route influences upper airway muscle activity in awake normal adults

1989 ◽  
Vol 66 (4) ◽  
pp. 1766-1771 ◽  
Author(s):  
R. C. Basner ◽  
P. M. Simon ◽  
R. M. Schwartzstein ◽  
S. E. Weinberger ◽  
J. W. Weiss
Keyword(s):  
Muscle Activity ◽  
Minute Ventilation ◽  
Statistical Significance ◽  
Upper Airway ◽  
Mouth Breathing ◽  
Emg Activity ◽  
Electromyographic Activity ◽  
Bipolar Electrodes ◽  
Inspiratory Resistance ◽  
Topical Nasal Anesthesia

Both nasal obstruction and nasal anesthesia result in disordered breathing during sleep in humans, and bypassing the nasal route during tidal breathing in experimental animals produces decreased electromyographic activity of upper airway (UA) dilating muscles. To investigate UA responses to breathing route in normal awake humans, we studied eight healthy males (ages 21–38 yr) during successive trials of voluntary nose breathing (N), voluntary mouth breathing (M), and mouth breathing with nose occluded (MO). We measured genioglossus electromyographic activity (EMGgg) with perorally inserted bipolar electrodes, alae nasi (EMGan) and diaphragm EMG activity (EMGdi) with surface electrodes, and minute ventilation (VE) with a pneumotachograph. Mean phasic inspiratory EMG activity of both UA muscles was significantly greater during N than during M or MO, even when a 2.5-cmH2O.l-1.s inspiratory resistance was added to MO (P less than 0.01). In contrast, neither EMGdi nor VE was consistently affected by breathing route. EMGgg during N was significantly decreased after selective topical nasal anesthesia (P less than 0.002); a decrease in EMGan did not achieve statistical significance. These data suggest that peak UA dilating muscle activity may be modulated by superficial receptors in the nasal mucosa sensitive to airflow.

Effects of thoracic dorsal rhizotomies on the respiratory pattern in anesthetized cats

1977 ◽  
Vol 43 (1) ◽  
pp. 20-26 ◽  
Author(s):  
R. Shannon
Keyword(s):  
Tidal Volume ◽  
Respiratory Activity ◽  
Respiratory Rhythm ◽  
Respiratory Pattern ◽  
Thoracic Wall ◽  
Intercostal Muscle ◽  
Inspiratory Time ◽  
Expiratory Time ◽  
Intercostal Muscles ◽  
Dorsal Roots

Experiments were conducted to determine if thoracic wall proprioceptor afferents are involved in the modulation of respiratory activity during eupnea. The effects of elimination of thoracic wall afferents (thoracic dorsal rhizotomies (TDR) on tidal volume (VT), frequency (f), inspiratory time (ti) and expiratory time (te) were studied in vagotomized cats anesthetized with diallylbarbituric acid (Dial). Dorsal rhizotomies 1–12 resulted primarily in a decreased VT and ti, and an increased f. Further experiments were performed to determine if these changes in respiratory pattern could be correlated with known reflexes from the middle and lower intercostal muscles, or lungs, via thoracic dorsal roots. Afferents from these sources were eliminated by TDR 5–9, 10–13, and 1–4. TDR 1–4 had no significant effect on the respiratory pattern. TDR 5–9 and TDR 10–13 produced changes similar in direction to TDR 1–12. The results indicate that: a) afferents 1–4 from the upper intercostal muscles and lungs (sympathetic afferents) do not contribute significantly to the control of the spontaneous respiratory rhythm, and b) afferents via the middle thoracic roots, 5–9, and the lower thoracic roots, 10–13, contribute significantly to the rhythm. The results do not completely correlate with known intercostal reflexes, but it is suggested that elimination of intercostal muscle proprioceptor afferents is responsible for the observed effects of thoracic dorsal rhizotomies.

Prostaglandin synthesis blockade by ketoprofen attenuates respiratory and cardiovascular responses to static handgrip

1995 ◽  
Vol 78 (2) ◽  
pp. 449-457 ◽  
Author(s):  
G. A. Fontana ◽  
T. Pantaleo ◽  
F. Bongianni ◽  
F. Cresci ◽  
F. Lavorini ◽  
...  
Keyword(s):  
Tidal Volume ◽  
Minute Ventilation ◽  
Maximum Voluntary Contraction ◽  
Cardiovascular Responses ◽  
Inspiratory Flow ◽  
Prostaglandin Synthesis ◽  
Respiratory Frequency ◽  
Placebo Control ◽  
Electromyographic Activity ◽  
End Tidal

We investigated the effects of prostaglandin synthesis blockade on the changes in breathing pattern, mean blood pressure (MBP), and heart rate (HR) elicited by 3 min of static handgrip at 30% of the maximum voluntary contraction in 12 healthy volunteers. Before each handgrip trial, subjects were treated with intravenous administration of either saline placebo (control) or 1 mg/kg of ketoprofen. Muscle tension and integrated electromyographic activity of exercising muscles remained fairly constant during each trial. In agreement with our earlier findings, during control handgrip minute ventilation progressively increased (P < 0.01) due to a rise in tidal volume and, to a lesser extent, in respiratory frequency. Mean inspiratory flow, MBP, and HR also increased (P < 0.01). End-tidal PCO2 decreased (P < 0.05) during the late phases of control handgrip bouts. Ketoprofen administration reduced serum thromboxane B2 levels (from 57.5 +/- 7.0 to 1.6 +/- 0.4 pg/ml; P < 0.01) and significantly attenuated mean increases in minute ventilation (40.25 +/- 0.60%), tidal volume (37.78 +/- 7.48%), respiratory frequency (55.94 +/- 17.92%), inspiratory flow (42.66 +/- 5.11%), MBP (22.33 +/- 6.82%), and HR (11.04 +/- 2.75%) during the 3rd min of handgrip. End-tidal PCO2 remained close to normocapnic levels. In agreement with previous animal investigations, the present results show that arachidonic acid metabolites are involved in the regulation of the cardiovascular responses to static efforts in humans, possibly through a stimulatory action on muscle receptors. Furthermore, they provide the first experimental evidence that products of the cyclooxygenase metabolic pathway play a role in the mediation of the respiratory adjustments elicited by this form of exercise.

Effect of Almitrine on Ventilation and on Diaphragm and Geniohyoid Muscle Activity in the Rat

1996 ◽  
Vol 91 (3) ◽  
pp. 337-345 ◽  
Author(s):  
Ken D. O'halloran ◽  
Aidan K. Curran ◽  
Aidan Bradford
Keyword(s):  
Tidal Volume ◽  
Muscle Activity ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Laryngeal Nerve ◽  
Respiratory Frequency ◽  
Diaphragm Muscle ◽  
Arterial Blood

1. Ventilation was measured during normoxia, hypoxia and hypercapnia before and after administration of almitrine in conscious, unrestrained, tracheostomized rats with the superior laryngeal nerves intact or cut. In superior laryngeal nerve-intact animals breathing air, almitrine increased minute ventilation due to an increase in respiratory frequency with no change in tidal volume. In superior laryngeal nerve-sectioned animals, the minute ventilatory response to almitrine was reduced due to a reduced tidal volume component of the response. Almitrine increased the ventilatory response to hypercapnia in superior laryngeal nerve-intact but not in sectioned animals. 2. In anaesthetized, vagotomized rats breathing spontaneously through a low-cervical tracheostomy, diaphragm and geniohyoid electromyographic activities were recorded. Arterial blood pressure and rectal temperature were continuously monitored. A single dose of almitrine was administered intravenously. In all animals, the geniohyoid muscle had phasic inspiratory activity which slightly preceded diaphragm activity. Almitrine had no effect on respiratory frequency or inspiratory and expiratory duration but increased mean peak integrated diaphragm (+29.3 ±13.6%) and geniohyoid (+ 132.0 ±21.3%) muscle activity. 3. These results show that almitrine exerts part of its ventilatory effects through superior laryngeal nerve afferents. Almitrine preferentially excites upper airway compared with diaphragm muscle activity, suggesting a potential role in the alleviation of obstructive apnoea.

Effects of expiratory threshold loading during steady-state exercise

1975 ◽  
Vol 39 (5) ◽  
pp. 697-701 ◽  
Author(s):  
I. Goldstein ◽  
S. Goldstein ◽  
J. A. Urbanetti ◽  
N. R. Anthonisen
Keyword(s):  
Steady State ◽  
Tidal Volume ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Bicycle Ergometer ◽  
Inspiratory Capacity ◽  
Mouth Pressure ◽  
Consistent Change ◽  
Residual Capacity ◽  
Response To Exercise

Increases in functional residual capacity (FRC) decrease inspiratory muscle efficiency; the present experiments were designed to determine the effect of FRC change on the ventilatory response to exercise. Six well-trained adults were exposed to expiratory threshold loads (ETL) ranging from 5 to 40 cmH2O during steady-state exercise on a bicycle ergometer at 40–95% VO2max. Inspiratory capacity (IC) was measured and changes of IC interpreted as changes of FRC. ETL did not consistently limit exercise performance. At heavy work (greater than 92% VO2max) minute ventilation decreased with increasing ETL; at moderate work (less than 58% VO2max) it did not. Decreases in ventilation were due to decreases in respiratory frequency with prolongation of the duration of expiration being the most consistent change in breathing pattern. At moderate work levels, FRC increased with ETL; at maximum work it did not. Changes in FRC were dictated by constancy of tidal volume and a fixed maximum end-inspiratory volume of 80–90% of the inspiratory capacity. When tidal volume was such that end-inspiratory volume was less than this value, FRC increased with ETL. Mouth pressure measured during the first 0–1 s of inspiratory effort against an occluded airway (P0-1) was increased by ETL equals 30 cmH2O, in spite of the fact that ventilation was decreased. We concluded that changes in FRC due to ETL had no effect on the ventilatory response to exercise and that changes in P0-1 induced by ETL did not reflect changes of inspiratory drive so much as changes of the pattern of inspiration.

Effects of negative upper airway pressure on pattern of breathing in sleeping infants

1989 ◽  
Vol 66 (4) ◽  
pp. 1599-1605 ◽  
Author(s):  
B. T. Thach ◽  
A. P. Menon ◽  
G. L. Schefft
Keyword(s):  
Tidal Volume ◽  
Airway Pressure ◽  
Upper Airway ◽  
Face Mask ◽  
Inhibitory Effect ◽  
Lower Airway ◽  
Quiet Sleep ◽  
Reflex Mechanism ◽  
Inspiratory Muscles ◽  
Reflex Latency

Negative upper airway (UAW) pressure inhibits diaphragm inspiratory activity in animals, but there is no direct evidence of this reflex in humans. Also, little is known regarding reflex latency or effects of varying time of stimulation during the breathing cycle. We studied effects of UAW negative pressure on inspiratory airflow and respiratory timing in seven tracheostomized infants during quiet sleep with a face mask and syringe used to produce UAW suction without changing lower airway pressure. Suction trials lasted 2–3 s. During UAW suction, mean and peak inspiratory airflow as well as tidal volume was markedly reduced (16–68%) regardless of whether stimulation occurred in inspiration or expiration. Reflex latency was 42 +/- 3 ms. When suction was applied during inspiration or late expiration, the inspiration and the following expiration were shortened. In contrast, suction applied during midexpiration prolonged expiration and tended to prolong inspiration. The changes in flow, tidal volume, and timing indicate a marked inhibitory effect of UAW suction on thoracic inspiratory muscles. Such a reflex mechanism may function in preventing pharyngeal collapse by inspiratory suction pressure.

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